There are presently no pharmacological methods to regulate the formation of βArrestin based signaling complexes without affecting G-protein mediated signaling. Current drugs acting on GPCRs are either receptor agonists (bromocriptine, apomorphine) receptor antagonists (haloperidol, beta-adrenergic blocking agents) or indirect agonists (amphetamines, selective serotonin reuptake inhibitor, methylphenidate), that exert their effects on all components of GPCR signaling. As a result of this lack of signaling-mechanism specificity, current compounds can alleviate symptoms resulting from aberrant βArrestin-based signaling while leading to the development of side effects through concomitant deregulation of G-protein mediated signaling. Conversely, the therapeutic action of these drugs can also come from their action on G-protein mediated signaling while side effects would arise from noxious effects of βArrestin-based signaling complexes. Thus, alone or in combinations, drugs acting on the formation of βArrestin-based signaling complexes provide more specific ways to regulate GPCR signaling then currently available compounds. A variation of this theme would be compounds that would bind to GPCRs specifically but would act differentially as agonists or antagonists for one response (i.e. G protein-dependent signaling) and not the other (βArrestin-dependent signaling) and vice versa. No such compounds are known yet for receptors like those for dopamine, serotonin, adrenergic alpha, beta, but could be identified by the methods outlined herein.